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100 Cards in this Set
- Front
- Back
abrupt onset and termination
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paroxsymal
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SVT characteristics
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paroxsymal
>180BPM Pwave hidden in QRS reg rhythm normal QRS |
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origination of eptopic focus is above bifurcation of bHIS
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SVT
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causes of SVT in normal heart
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overexertion
emotional stress stimulants dig tox cor pulmonale CAD RHD |
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tx for SVT
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vag maneuvers
adenosine verapamil cardioversion |
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when is direct cardioversion used for SVT
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when vag maneuvers and drugs do not work
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how is adenosine given
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6 mg rapid followed with 20ml NS
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what happens if no results after first dose of adenosine
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give 12 mg rapid followed by bolus of NS
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SE of adenosine
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flushing
chest pain/tightness brief asystole bradycardia |
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PAC
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atria firing early
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contractions originating from ectopic focus in atrium from somewhere other than SA node
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PAC
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what causes PAC
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waves travel across atria by abnormal pathway creating distorted p wave
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rate of PAC
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reg except where PAC is
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causes of PAC
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emotional stress
caffeine/tobacco/ETOH hypoxia drugs electrolyte imbalances COPD valvular disease |
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when are PACs a concern
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in ppl with heart disease d/t to possible sign of more serious dysrhythmia
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tx for PAC
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b-adrenergic blocker
diltiazem (cardizem) propafenone (rhythmol) amiodarone flecanide (tambicor) clonidine (catapres) MG |
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recurring regular saw tooth shaped flutter waves
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a flutter
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what does a flutter cause
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blood to pool in atria d/t weak contractions
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a flutter characteristics
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250-350bpm
from single ectopic focus vent rate reg or irreg QRS normal |
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concern for a flutter
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hih vent rates and loss of atrial kick can decrease CO
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serious risk with a fluter
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stroke
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causes of a flutter
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atrial stretching
CAD ETOH pericarditis HTN mitral valver dis. PE chronic lung dis cardiomyopathy hyper thyroid dig/ quinidine/epi |
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clinical sx of a flutter
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palpitations
decreased CO CHF |
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tx for a flutter
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b adrenergic blockers
cardizem rhythmol amiodarone flecinide clonidine |
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drugs that slow HR
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CCB
b adrenergic blockers |
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other tx for a flutter
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cardioversion
radiofrequency catheter ablation |
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long term tx of choice for a flutter
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ablation
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results d/t multiple ectopic foci resulting in loss of atrial contraction
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a fib
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twitching of atria
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a fib
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charac of a fib
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p wave not recognizable
cant measure PR irregular atrial rate > 350 |
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causes of a fib
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ETOH intox
cafffeine electrolytes cardiac surg |
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can result from a fib
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thrombi
embolus decrease CO |
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tx for a fib
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decrease vent response
prevent embolic stroke dig/ CCB/ BAB heparin coumadin (long term) |
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if pt is in a fib for >48hrs what is recommended b4 cardioversion
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anticoag therapy with warfarin for 3-4 wks before and 4-6 wks after
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other tx for a fib
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radiofrequency ablation
maze procedure |
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contraction originating in ectopic focus of the vents
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PVC
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characteristics of PVC
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wide and distorted QRS
a pause may follow Pwave not visible |
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multifocal PVC
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more than one place firing
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unifocal PVC
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one place firing with them looking similar
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Q 3rd beat is PVC
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trigeminy
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q 2nd beat it PVC
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bigeminy
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why is pwave absent with PVC
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not firing from sa node
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tx for PVC
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oxygen
electrolyte replacement drugs |
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run of 3 or more PVC
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vent tach
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characteristics of vtach
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150-250 bpm
monomorphic/polymorphic sustained/unsustained pulsatile/unpulsatile |
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why is there no pwave with v tach
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rapid vent firing
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causes of v tach
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Mi
CAD hypoxia bradycardia drugs electrolyte imb long Qt syndrome dig tox CNS disorders |
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tx for pulseless vtach
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CPR
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causes of v fib
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acute mi
CAD hyperkalemia hypoxia acidosis drug toxicity |
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class 1
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na channel blockers
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what do the class 1 drugs slow
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atria
vents Bhis |
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class 1A drugs
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quinidine
procainamide disopyramide |
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what do the class 1A drugs do
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widen QRS
prolong QT reduce automaticity prolong refrac. period |
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nsg imps for class 1 a
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mtr cardiac rhythm
monitor bp |
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class 1b drugs
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lidocaine
mexiletine phenytoin |
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what do class 1 B drugs do
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supress automaticityin
- Bhis -fibers - |
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class 1 a drugs do what
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supress dysrhytmia
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SE of class 1B
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difficulty breathing/swallowing
convulsions resp dep neurotoxicity cardiovascular collapse |
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nsg imp for class 1 B
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mtr bp/ ecg cont.
resp and neuro status mtr serum blood levels |
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when should 1B drugs be stopper
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prolonged PR or QRS
new dysr |
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slows conduction velocity and increases vent refractoriness
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class 1 C
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class 1 C drugs
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flecanide
propafenone |
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nsg imp for class 1 C
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correct K levels before giving
mtr serum blood levels |
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action of class 2
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block effects of epi
decrease SA automaticity slow av conduction slow myocardial contractility |
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drugs of class 2
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propanolol
esmolol acebutolol |
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SE of class 2
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anaphylactic reaction
steven johnson syn laryngospasm bronchoconstriction bradycardia |
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nsg imp for class 2
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mtr VS before and after
mtr for hypotension |
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Class 3
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K channel blockers
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class 2
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beta blockers
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effect of class 3
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prolong duration of action potential refrac period
txs life threat- vent dys, SVT and a fib |
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SE of class 3
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hypotension
dizziness sinus arrest |
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class 3 drugs
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amiodarone
bretylium sotalol ibutilide dofetilifde |
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nsg imp for class 3
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correct K and Mg before
mtr for hypotension long half life |
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class 4
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Ca channel blockers
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drugs for class 4
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verapamil
diltiazem digitalis adenosine |
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actions of class 4
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reduce automaticity in SA
slow conduction in AV |
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SE of class 4
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hypotension
av block |
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nsg imp for class 4
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correct k and mg
mtr serum drug levels |
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junctional characteristics
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originates in av node area
sa failed to fire or blocked at av 40-60bpm may or may not have p wave |
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causes of junctional
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cad
heart failure cardiomayopathy electrolyte imb inferior mi RHD drugs |
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accelerated junctional
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60-100
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junctional tach
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100-250
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arrythimias frin delayed or failed conduction of supravent impulses to vents
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av block
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every impulse is conducted to the vents but duration of av conduction is prolonged
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first degree
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first degree charac
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PR > .20
each p wave has qrs pr interval is constant |
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causes of type 1 block
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Mi
cad rhd hyperthy vag stim drugs |
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gradual lenghthening of PR and eventually qrs is dropped
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second degree type 1
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causes of second degree type 1
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dig
BAB CAD |
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pwave not conducted and pr stays the same
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second degree type 2
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causes of 2nd type 2
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RHD
cad anterior MI dig tox |
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often progresses to 3 degree
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2nd type 2
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tx for 2nd type 2
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pacemaker
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has a vent escape
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third degree
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lacks t waves
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3rd degree
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tx for 2nd type 2
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pacemaker
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form of av dissociation in which no impulses from the atria are conducted to the vents
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3rd degree
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abnormal cardiac rhythms
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dysrhythmias
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output of defib measured in what
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joules
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360 joules
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monophasic defib
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150-200 joules
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biphasic defib
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